Importantly, such insights can now guide studies that focus on the normal function and interactions of these proteins and how they might be enhanced by disease-causing mutations. These studies could give better understanding of how the proteins cause disease.

We had known that the expansion of the glutamine tract within Ataxin-1 probably interfered with normal clearance of Ataxin-1, meaning that it accumulated in cells.

The overall picture we have now is that glutamine expansion causes some aspects of the pathology of SCA1 in part by enhancing the activity of the domain that is outside the glutamine repeat.

We had been accumulating clues that the glutamine tract expansion is clearly what is important for disease because that's the mutation. But we also concluded that there was something else beyond the glutamine that's really mediating the toxicity of the protein.

It's still a required class -- it's not like it's going to be super-fun -- but at least you're getting stuff out of the way quicker, and getting prepared.

אל תחשוב שהסודות הגדולים האלה ידועים עד תכליתם וסופם לאחד מאתנו. לא! אלא שפעמים האמת מבהיקה לנו עד שאנו חושבים אותה לאור יום. אחרי-כן החומרים וההרגלים חוזרים ומסתירים אותה עד שאנו חוזרים להיות בלילה אפל, קרוב למה שהיינו בתחילה.